DIURNAL-VARIATIONS OF SEROTONIN AND DOPAMINE LEVELS IN DISCRETE BRAIN-REGIONS OF SYRIAN-HAMSTERS AND THEIR MODIFICATION BY CHRONIC CLORGYLINE TREATMENT

Citation
N. Ozaki et al., DIURNAL-VARIATIONS OF SEROTONIN AND DOPAMINE LEVELS IN DISCRETE BRAIN-REGIONS OF SYRIAN-HAMSTERS AND THEIR MODIFICATION BY CHRONIC CLORGYLINE TREATMENT, Brain research, 627(1), 1993, pp. 41-48
Citations number
43
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00068993
Volume
627
Issue
1
Year of publication
1993
Pages
41 - 48
Database
ISI
SICI code
0006-8993(1993)627:1<41:DOSADL>2.0.ZU;2-S
Abstract
In Syrian hamsters, chronic administration of the type A monoamine oxi dase inhibitor, clorgyline (CLG), alters the intrinsic period and dail y pattern of the circadian rhythm of wheel running, and changes the in tensity-response curve for phase-shifting of the rhythm by light pulse s. Chronic treatment with CLG also decreases hypothalamic and peritone al temperatures, particularly during the rest phase of the activity-re st cycle. To help identify monoamines that may mediate CLG's effects o n circadian rhythms, we measured levels of dopamine (DA) and serotonin (5-HT) at nine time points over a 24-h period in micro-dissected brai n regions in chronic CLG-treated or saline-treated hamsters. For 5-HT, a diurnal variation was detected in all regions in saline-treated ani mals; for DA, no diurnal variation was detected in any region. In all regions. 5-HT levels and, to a lesser extent, DA levels were higher af ter CLG treatment. The acrophase of the 5-HT rhythm in the suprachiasm atic nucleus (SCN) was delayed by CLG-treatment, while the acrophase i n the dorsal raphe nucleus was unchanged. The diurnal variation of 5-H T in the paraventricular nucleus of the hypothalamus, medial preoptic area, and median raphe nuclei was no longer detectable after chronic C LG-treatment. The phase-delay induced by CLG treatment in the daily rh ythm of serotonin levels in the SCN, which functions as a circadian pa cemaker, may be an important mechanism underlying the drug's capacity to slow the intrinsic rhythm of the pacemaker and to phase-delay behav ioral rhythms that are under its control.